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Rapid Evaluation of Toxicity of Chemical Compounds Using Zebrafish Embryos
Published on: August 25, 2019
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Trace-level Gabapentin can induce cardiovascular developmental toxicity through apoptosis in zebrafish larvae
Yide He1, Jun Hu1, Rosa Freitas2
1School of Environmental Science and Engineering, Nanjing Tech University, Jiangsu, 211816, PR China; Sino-Portuguese Joint International Laboratory of Aquatic Toxicology, Nanjing Tech University, 30 South Puzhu Road, Nanjing, 211816, Jiangsu Province, PR China.
Environmental Pollution (Barking, Essex : 1987)
|July 11, 2024
Summary
Gabapentin (GBP) harms zebrafish cardiovascular systems by altering blood flow and vessel development. These effects, linked to oxidative stress, were reversed by N-acetyl-L-cysteine, indicating potential aquatic toxicity pathways.
Area of Science:
- Environmental toxicology
- Aquatic ecotoxicology
- Pharmacology
Background:
- Gabapentin (GBP), an antiepileptic drug, is an emerging aquatic pollutant.
- Previous studies indicated potential cardiac toxicity in zebrafish, but cardiovascular effects remain unclear.
Purpose of the Study:
- To assess the impact of environmental concentrations of Gabapentin on zebrafish cardiovascular systems during early development.
- To elucidate the mechanisms underlying Gabapentin's cardiovascular toxicity in aquatic organisms.
Main Methods:
- Zebrafish embryos were exposed to Gabapentin (0, 0.1, 10, 1000 μg/L).
- Cardiovascular parameters (heart rate, blood flow, vascular width) were measured.
- Gene expression related to angiogenesis and apoptosis was analyzed.
- Reactive oxygen species (ROS) and antioxidant levels were quantified.
- Reversibility of effects was tested using N-acetyl-L-cysteine.
Main Results:
- Gabapentin exposure increased heart rate and blood flow.
- Vascular development was impaired, with decreased vascular width at 10 μg/L and higher.
- Gabapentin inhibited key angiogenesis genes (flk1, vegfr-3, gata1, vegfα, vegfr-2).
- Increased ROS and antioxidant enzyme levels were observed at 0.1 μg/L.
- Vascular cell apoptosis was promoted via p53, bad, and bcl2 pathways.
- Adverse effects were reversible with N-acetyl-L-cysteine treatment.
Conclusions:
- Gabapentin induces cardiovascular toxicity in zebrafish, characterized by altered hemodynamics and abnormal vascular development.
- Oxidative stress and vascular cell apoptosis play critical roles in Gabapentin's toxicity.
- The reversibility of effects with an antioxidant suggests a viable pathway for mitigating Gabapentin's ecotoxicological impact.
